Possible involvement of endothelin-1 and nitric oxide in the pathogenesis of proliferative diabetic retinopathy.
Autor: | Oku H; Department of Ophthalmology, Osaka Medical College, Osaka, Japan. hidehirookku@aol.com, Kida T, Sugiyama T, Hamada J, Sato B, Ikeda T |
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Jazyk: | angličtina |
Zdroj: | Retina (Philadelphia, Pa.) [Retina] 2001; Vol. 21 (6), pp. 647-51. |
DOI: | 10.1097/00006982-200112000-00013 |
Abstrakt: | Background: Overproduction of endothelin-1 (ET-1) and nitric oxide (NO) in the retina is demonstrated in experimental diabetic animals. To clarify the possible involvement of ET-1 and NO in the pathogenesis of diabetic retinopathy, the authors examined the vitreous levels of these principal endothelium-derived vasoactive substances in patients with proliferative diabetic retinopathy (PDR). Methods: Vitreous fluid was taken from patients with PDR (ET-1, n = 12; NO, n = 12) and from patients with macular holes as controls (ET-1, n = 10; NO, n = 10) at vitreous surgery. Endothelin-1 and NO metabolites were measured by radioimmunoassay and high-performance liquid chromatography based on the Griess method, respectively. Results: Endothelin-1 levels (mean +/- SE) were 21.5 +/- 1.7 pg/mL in the vitreous of patients with PDR and 16.7 +/- 0.7 pg/mL in the vitreous of patients with macular hole. There was a significant difference between patients with PDR and controls (P = 0.009, Mann-Whitney). Nitrate (NO3) was 49.8 +/- 5.0 micromol/L in patients with PDR and 24.2 +/- 2.8 micromol/L in patients with macula hole; it was also significantly elevated in patients with PDR (P = 0.004, Mann-Whitney), whereas nitrite (NO2) was not detected in this study. Conclusion: These results indicate that ET-1 and NO may be related in the pathogenesis of PDR. |
Databáze: | MEDLINE |
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